Astrocyte- and Microglia-Specific Mitochondrial DNA Deletions Levels in Sporadic Alzheimer's Disease

J Alzheimers Dis. 2019;67(1):149-157. doi: 10.3233/JAD-180661.

Abstract

Oxidative stress is implicated in the pathogenesis of neurodegenerative diseases, including sporadic Alzheimer's disease (AD). Mitochondrial DNA (mtDNA) deletions are markers of oxidative damage with an age-dependent accumulation. In a previous study, we analyzed mtDNA levels in diverse neuronal cell types in order to unravel the impact of oxidative stress in brains of AD patients. The aim of this study was to identify possible correlations between mtDNA deletion levels of selected astrocytes and microglia from three brain regions with different vulnerability to AD pathology and different stages of disease compared to controls. Our results reflect a higher vulnerability of hippocampal astrocytes and microglia to oxidative stress compared to other brain regions, such as cerebellum and brainstem.

Keywords: Alzheimer’s disease; astrocytes; brainstem; cerebellum; hippocampus; microglia; mitochondrial DNA; oxidative stress; selective vulnerability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / genetics*
  • Astrocytes / metabolism*
  • Brain Stem / cytology
  • Brain Stem / metabolism
  • Cerebellum / cytology
  • Cerebellum / metabolism
  • DNA, Mitochondrial / genetics*
  • Female
  • Gene Deletion
  • Hippocampus / cytology
  • Hippocampus / metabolism
  • Humans
  • Immunohistochemistry
  • Male
  • Microglia / metabolism*
  • Middle Aged
  • Oxidative Stress / genetics

Substances

  • DNA, Mitochondrial